The effects of large changes in hemoglobin concentration were studied in rainbow trout in fresh water between 8 and 14 C. Anemia was produced by injecting phenylhydrazine hydrochloride or by replacing blood with either saline or plasma.No significant changes were observed in the rate of oxygen consumption, arterial or venous oxygen tensions, ventilation volume, inspired and expired water oxygen tensions, or dorsal aortic blood pressure. The primary compensatory mechanism invoked was an increase in the cardiac output, which was accomplished almost entirely by increases in stroke volume. Although the viscosity of the blood was reduced, there must also be large changes in the peripheral resistance to blood flow, since greatly increased cardiac output was achieved without significant increase in blood pressure.The change in blood oxygen capacity and increase in cardiac output caused significant lowering of the ventilation–perfusion ratio, but the capacity–rate ratio of water to blood varied only a little. A small rise occurred at low hematocrit values, due to small changes in a number of parameters.The experiments illustrate what happens when blood oxygen capacity is reduced, but do not elucidate the mechanism for control of stroke output of the heart. They also indicate that a species' hemoglobin level is maintained at a level that allows cardiac output to vary over an optimal range of its efficiency curve.